This is one of the most important systems for the human. It extends from the mouth to the anus. The each individual organ has a distinct function and the functions are compartmentalized with the aid of specialized independently controlled thickened sphincters. The gut wall consists of well defined layers and these layers contribute to the functional activities in each region. The mucosa serves as a barrier to luminal contents or as a site for transfer of fluids or nutrients. Gut smooth muscle mediates propulsion from one region to the next. Many GI organs possess a serosal layer that not only provides a supportive foundation but also permits external input.
Pancreaticobiliary conduits deliver bile and enzymes into the duodenum. A rich vascular supply is modulated by GI tract activity. Lymphatic channels assist in gut immune activities. Intrinsic gut wall nerves provide the basic controls for propulsion and fluid regulation. Extrinsic neural input provides volitional or involuntary control to degrees that are specific for each gut region.
2. Functions of the GI tract
The GI tract serves two main functions;
I. Assimilation of nutrients and
II. Elimination of waste.
The gut anatomy is organized to serve these functions. In the mouth, food is processed, mixed with salivary amylase, and form a food bolus which is delivered to the stomach by propulsion of esophagus. The stomach further process the food boluses by triturating and mixing with pepsin and acid., the stomach also secretes intrinsic factor for vitamin B12 absorption.
The small intestine is the site where most of the absorption takes place Triturated food from the stomach is mixed with pancreatic juice and bile in the proximal duodenum to facilitate digestion. Pancreatic juice contains the main enzymes for carbohydrate, protein, and fat digestion as well as bicarbonate to optimize the pH for activation of these enzymes. Bile secreted by the liver and stored in the gallbladder is essential for intestinal lipid digestion.
The colon prepares the waste material for controlled evacuation. The colonic mucosa dehydrates the stool, decreasing daily fecal volumes from the 1000 to 1500 mL delivered from the ileum to the 100 to 200 mL expelled from the rectum.
3. Extrinsic modulation of gut function
Since the gut is in physical continuity with the outside environment, it needs specialized protective mechanism to act against deleterious effects of consumed foods, medications, toxins, and infectious organisms. Mucosal immune mechanisms include a lymphocyte and plasma cell population that resides in the epithelial layer and lamina propria backed up by lymph node chains to prevent noxious agents from entering the circulation. All substances absorbed into the bloodstream are filtered through the liver via the portal venous circulation. In the liver, many drugs and toxins are detoxified by a variety of mechanisms.
Although intrinsic nerves control most basic gut activities, extrinsic neural input modulates a number of functions. The two activities under voluntary control are swallowing and defecation.
4. Overview of gastrointestinal diseases
The cause of the GI disease could be inside or outside and the severity of the condition could range from mild self limiting to severe wit intractable symptoms. Diseases may be localized to a single organ or exhibit diffuse involvement at a number of sites.
Classification of GI diseases; GI diseases are manifestations of alterations in nutrient assimilation or waste evacuation or in the activities supporting these main functions.
I. Impaired Digestion and Absorption; Diseases of the stomach, intestine, Biliary tree and pancreas can cause alteration of nutrient digestion and absorption.( maldigestion syndrome, Zollinger-Ellison syndrome, lactose deficiency, )
II. Altered Secretion; Selected GI diseases result from alteration of gut secretion (Gastric acid hypersecretion occurs in Zollinger-Ellison syndrome, G-cell hyperplasia, retained antrum syndrome. Conversely, patients with atrophic gastritis or pernicious anemia release little or no gastric acid)
III. Altered Gut Transit; Alterations in gut transit are commonly secondary to mechanical obstruction (stricture or neoplasm, Gastric outlet obstruction, rectal prolepses, intussusceptions disordered gut motor function).
IV. Immune Dysregulation; Many inflammatory GI conditions are consequences of altered gut immune function (celiac disease, Eosinophilic gastroenteritis, Ulcerative colitis and Crohn’s disease).
V. Impaired Gut Blood Flow; Different GI regions are at variable risk for ischemic damage from impaired blood flow (arterial embolus; arterial thrombosis, venous thrombosis; or hypoperfusion from dehydration, sepsis, hemorrhage, or reduced cardiac output).
VI. Neoplastic Degeneration All GI regions are susceptible to malignant degeneration to varying degrees (colorectal cancer, , lymphomas)
VII. Disorders without Obvious Organic Abnormalities; The most common GI disorders show no abnormalities on biochemical or structural testing and include irritable bowel syndrome (IBS), functional dyspepsia, non cardiac chest pain, and functional heartburn.
Symptoms of gastrointestinal disease; The most common GI symptoms are abdominal pain, heartburn, nausea and vomiting, altered bowel habits, GI bleeding, and jaundice dysphagia, anorexia, weight loss, fatigue, and extra intestinal symptoms.
5. Investigations of GI tract diseases
a) Investigations of steatorrhoea
Screening tests; a number of screening tests are available. But there is an overlap between the normal and the abnormal. Therefore these are rarely used
I. Plasma carotene; low levels are detected in plasma in malabsorption. It is also low in plasma in conditions like liver diseases and low intake of vegetables.
II. Plasma optical density; 60g of fat is ingested as buttered toast and plasma optical density (620nm) is read hourly for 4 hours. Normal fat absorption is associated with a rise in the optical density of greater than 0.1
III. Plasma triglycerides; the level of plasma triglycerides is measured hourly for 4 hours after 60g fat load. Under normal conditions the maximum plasma triglycerides is achieved within 2-4 hours after fat ingestion.
IV. Vitamin A absorption; this is a fat soluble vitamin therefore its absorption is impaired in fat malabsorption.
V. 14-carbon labeled triglycerides test; the 14C labeled triolein is ingested and excretion of 14carbon dioxide in exhaled air is measured. This test is becoming a popular test as a quick and sensitive test of fat malabsorption.
Fecal fat test; this is the most reliable method of detecting steatorrhoea. In normal subject on a fat free diet the total output is 3g/day (source is intestinal secretions, mucosal cells and normal bacterial flora). On a normal diet (containing 75g of fat/day) the daily output of fecal fat is less than 7g/day.This implies that 90% of ingested fat is absorbed. To have a reliable results, diet must contain sufficient amount of fat 9 75g/day) for several days and bowel movements must be regular and collection should be over a minimum period of 3 days.
b) Investigations of protein malabsorption
Fecal nitrogen; normal nitrogen excretion is less than 2.5g/day with a 75g/day protein intake. This is increased in protein malabsorption and protein loosing enteropathy. But this investigation is not commonly performed.
c) Investigations of carbohydrates malabsorption
Xylose absorption test; Xylose is a pentose sugar which is not a constituent of blood. It can be absorbed without digestion and is absorbed in upper small intestine .Xylose is not metabolized by the body so it is excreted by glomerular filtration as it absorbed.5g of Xylose dose is given orally after fasting overnight. Then urine is collected in two portions (after 2 and 3 hours of ingestion) over the next 5 hours. In a normal subject more than 23% of the dose appear in the urine collected over 5 hours, with half of this appearing in urine of the first 2 hour aliquot. In mild cases 5 hour excretion is normal but half of it is excreted in the later 3 hours.
Lactose tolerance test; 50g of lactose (1g/kg) is given orally and blood samples are taken as for oral GTT.
Fecal pH and sugars
Intestinal disaccharide assay; this gives the definitive diagnosis
Hydrogen breathe test; when a fermentable substance present in the intestine, bacteria ferments it and liberates hydrogen. Increased bacterial flora as in blind loops increases the excretion of hydrogen. This test can be performed with lactose and sucrose test meals to detect lactase and sucrase deficiency.
d) Investigations of vitamins malabsorption.
Schilling test; radioactive vitamin B12 is given orally and a large flushing dose of unlabeled B12 is given parenterally to saturate binding site. Over the next 24 hours the amount if radioactive B12 excretion is estimated. If the excreted amount is >5-8% of ingested amount, the intrinsic factor deficiency will be <> 0.76. The low levels indicate pancreatic insufficiency.
II. Bile salt breathe test; this test detects bacterial overgrowth of the small intestine. 14C labeled glycine conjugated bile salts are given orally and the expired air is analyzed for 14Carbon dioxide (14CO2) . In normal subjects the labeled bile salts are absorbed intact and re-excreted by the liver. If gut is contaminated by bacteria it converts bile salts into 14CO2. The lung excretion of 14CO2 is also increased and disease or resection of terminal ileum, as unabsorbed bile salts reach the colon where they are metabolized by normal colonic flora and absorbed.
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